No abstract

High-fidelity intracranial electrode arrays for recording and stimulating brain activity have facilitated major advances in the treatment of neurological conditions over the past decade. Traditional arrays require direct implantation into the brain via open craniotomy, which can lead to inflammatory tissue responses, necessitating development of minimally invasive approaches that avoid brain trauma. Here we demonstrate the feasibility of chronically recording brain activity from within a vein using a passive stent-electrode recording array (stentrode). We achieved implantation into a superficial cortical vein overlying the motor cortex via catheter angiography and demonstrate neural recordings in freely moving sheep for up to 190 d. Spectral content and bandwidth of vascular electrocorticography were comparable to those of recordings from epidural surface arrays. Venous internal lumen patency was maintained for the duration of implantation. Stentrodes may have wide ranging applications as a neural interface for treatment of a range of neurological conditions.

In a prospective study to analyse stroke topography and outcome in diabetics and to determine the prognostic value ofblood glucose and glycosylated haemoglobin estimation, we evaluated 176 patients with acute stroke. The patients were classified into four groups on the basis of history, fasting glucose, and glycosylated haemoglobin: euglycaemic patients with no history of diabetes, stress hyperglycaemia, newly diagnosed diabetics, and known diabetics. A high prevalence of undiagnosed diabetes was shown. No difference was found in the type or site of stroke between the four groups. No difference was found in the site of symptomatic or incidental lesions on computerised axial tomography. Patients with stress hyperglycaemia and known diabetics had more severe strokes. Mortality was higher in patients with stress hyperglycaemia, newly diagnosed diabetics, and the combined diabetes groups. This increased mortality was evident in the hyperglycaemic and diabetic groups, even after excluding patients with cerebral haemorrhage. Stroke severity and mortality also increased independently with blood glucose in the euglycaemic group. We conclude that there is a correlation between admission glucose concentration, diabetes, and poor stroke outcome, which may not be attributed to stroke type or location.Epidemiological and necropsy studies show that diabetic patients have a higher incidence of ischaemic stroke than non-diabetic patients.' 2 In the Framingham study the incidence of thrombotic stroke was 2-5 times higher in diabetic men and 3-6 times higher in diabetic women than in those without diabetes.3 Wolf and Kannell reported that even when other risk factors such as hypertension and ischaemic heart disease are taken into account diabetes remains an independent risk factor for stroke.4 Previous studies have found a range of prevalence of undiagnosed diabetes in acute stroke populations from 6%' to 42%6.The type and topography of diabetes-related cerebral infarction may differ from brain infarcts in non-diabetics. In a necropsy survey Kane and Aronson7 found that diabetics had more lacunar lesions when compared with non-diabetics, especially in the distribution of the parasagittal perforating arteries. Peress et al8 also reported a higher occurrence of lacunar infarcts in diabetics compared with non-diabetic patients. In the Harvard cooperative stroke registry,9 hypertension and diabetes were present respectively in 75% and 29% of lacunar cases and 71% and 43% of cases in the South Alabama population study.'o Several animal studies of experimental cerebral ischaemia have shown that hyperglycaemia increases the severity of ischaemic brain dam-

We reviewed the records of all children (younger than 16 years of age) who presented with a diagnosis of optic neuritis (ON) identified through the comprehensive records-linkage system at the Mayo Clinic and identified 94 cases between 1950 and 1988 with a documented history of idiopathic ON. Detailed follow-up information was available on 79 patients, with a median length of follow-up of 19.4 years. Life-table analysis showed that 13% of the 79 patients with isolated ON had progressed to clinically or laboratory-supported definite multiple sclerosis (MS) by 10 years of follow-up, 19% by 20 years, 22% by 30 years, and 26% by 40 years. Gender, age, funduscopic findings, visual acuity, or family history of either ON or MS did not predict the development of MS. The presence of bilateral sequential or recurrent ON increased the risk of developing MS (p = 0.002; hazard ratio = 5.09), whereas the presence of infection within 2 weeks before the onset of ON decreased the risk of developing MS (p = 0.060; hazard ratio = 0.24). This study of childhood ON supports the lower risk of recurrence and progression to MS compared with adults.